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Baicalin Suppresses Migration, Invasion and Metastasis of Breast Cancer via p38MAPK Signaling Pathway
被引:56
|作者:
Wang, Xiu-Feng
[1
]
Zhou, Qian-Mei
[1
]
Du, Jia
[1
]
Zhang, Hui
[1
]
Lu, Yi-Yu
[1
]
Su, Shi-Bing
[1
]
机构:
[1] Shanghai Univ Tradit Chinese Med, Res Ctr Tradit Chinese Med Complex Syst, Shanghai 201203, Peoples R China
关键词:
Baicalin;
breast cancer;
MDA-MB-231;
cell;
metastasis;
side effects;
SCUTELLARIA-BAICALENSIS;
MOLECULAR-MECHANISMS;
UP-REGULATION;
APOPTOSIS;
MMP-2;
EXPRESSION;
MT1-MMP;
KINASE;
GROWTH;
BAX;
D O I:
10.2174/18715206113139990143
中图分类号:
R73 [肿瘤学];
学科分类号:
100214 ;
摘要:
Metastasis is the major cause of death in breast cancer patients. In this study, we investigated the effects of baicalin, a natural compound, on cell migration, invasion and metastasis using human breast cancer MDA-MB-231 cell line as model system. Baicalin not only dose-dependently inhibited MDA-MB-231 cells migration and in vitro invasion, but also suppressed the tumor outgrowth and the pulmonary metastasis of MDA-MB-231 cells in xenograft model. Importantly, treatment of baicalin caused little change in body weight, liver and kidney function of recipient animals. Tumorigenesis-inhibitory effect is likely linked to the capability of baicalin to downregulate metalloproteinase (MMP)-2, MMP-9, urokinase-type plasminogen activator (uPA) and uPA receptor (uPAR) expression in MDA-MB-231 cells. As baicalin blocked p38 mitogen-activated protein kinase (MAPK) activity and treatment of p38MAPK inhibitor SB203580 led to the reduction of MMP-2, MMP-9, uPA and uPAR expressions, we concluded that baicalin suppresses the tumorigenecity of MDA-MB-231 cells by down-regulating MMP-2, MMP-9, uPA and uPAR expressions through the interruption of p38MAPK signaling pathway.
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页码:923 / 931
页数:9
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